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Körperliche Belastung, endogene Opiate und Schmerz

Physical exercise, endogenous opiates and pain regulation

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Abstract

A series of studies with humans as well as experiments carried out on animals have shown that physical exercise leads to temporary hypoalgesia. Reduced sensitivity to pain is not only demonstrable after long-distance exercise (such as a marathon run) but also during and after intensive physical exercise on a laboratory ergometer. In a double blind study (20 mg naloxone versus placebo) experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (β-endorphin, cortisol, and catecholamines) were measured in ten healthy athletic men before, during, and after physical exercise on a cycle ergometer. A significant pain threshold elevation during exercise was found for finger (Anova,p<0.004) and dental pulp stimulation (p<0.01). Hypoalgesia remained present after exercise was stopped and the initial pain threshold level was returned to approximately 60 minutes after the exercise. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (p<0.001) after exercise. Naloxone failed to affect pain thresholds and plasma β-endorphin did not correlate significantly with pain thresholds. The cause of the exercise-induced hypoalgesia is probably an activation of central pain inhibitory mechanisms by the “stimulus” of physical exercise (stimulation-induced analgesia). Central pain inhibitory systems are probably thereby activated by the stimulation of afferent nerves endings (group III and IV) in the skeletal muscle. The same trigger mechanism also plays a role as a release stimulus for hormones which are secreted in increased measure during physical exercise (catecholamines, pituitary hormones). Plasma β-endorphin is probably not directly involved in the exercise-induced hypoalgesia but is rather a “marker” for the activating of central analgesia mechanisms.

Zusammenfassung

Eine Reihe von Studien beim Menschen wie auch tierexperimentellen Untersuchungen können inzwischen zeigen, daß körperliche Belastung zu einer zeitweiligen Hypoalgesie führt. Minderempfindlichkeit gegenüber Schmerz ist dabei nicht nur nach Langstreckenbelastung nachweisbar, wie z.B. nach einem Marathonlauf, sondern auch während und nach intensiver körperlicher Ergometerbelastung im Labor. In einer eigenen Untersuchung wurden experimentell bestimmte Schmerzschwellen (elektrische Reizung intrakutan am Finger und an der Zahnpulpa) und Plasmahormone (β-Endorphin, Cortisol, Katecholamine) vor, während und nach körperlicher Belastung auf einem Fahrradergometer gemessen. Die Untersuchung erfolgte doppelblind nach 20 mg Naloxon i.v. bzw. nach Plazebo. Ein signifikanter Schmerzschwellenanstieg konnte unter körperlicher Belastung sowohl am Finger (Anova,p<0,004) als auch am Zahn (p<0,01) nachgewiesen werden. Die Schmerzschwelle blieb auch nach Abbruch der Belastung erhöht und hatte 60 min nach Belastung ihr Ausgangsniveau wieder erreicht. Auch die subjektive Einschätzung überschwelliger Schmerzstimuli auf einer visuellen Analogskala war nach Belastung signifikant erniedrigt. Naloxon hatte keinen signifikanten Einfluß auf die Schmerzschwellen, und β-Endorphin zeigte keine signifikante Korrelation mit der Schmerzschwellenerhöhung unter körperlicher Belastung. Ursache der belastungsinduzierten Hypoalgeise ist wahrscheinlich eine Aktivierung zentraler schmerzinhibitorischer Mechanismen durch den “Stimulus” körperliche Belastung (stimulationsinduzierte Analgesie). Zentrale schmerzinhibitorische Systeme werden dabei vermutlich durch die Reizung afferenter Nervenfasern (Gruppe III und IV) im Skelettmuskel aktiviert. Der gleiche Triggermechanismus spielt auch eine Rolle als Freisetzungsstimulus für Hormone, die unter körperlicher Belastung verstärkt ausgeschüttet werden (Katecholamine, Hypophysenhormone). Plasma-β-Endorphin ist wahrscheinlich nicht direkt an der belastungsinduzierten Hypoalgesie beteiligt, sondern eher “Marker” für eine Aktivierung zentraler Analgesiemechanismen.

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  1. Arzt für Innere Medizin und Kardiologie Benedikt Kreutz-Rehabilitationszentrum für Herz- und Kreislaufkranke, Südring 15, W-7812 Bad, Krozingen, Bundesrepublik Deutschland

    C. Droste

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Droste, C. Körperliche Belastung, endogene Opiate und Schmerz. Schmerz 5, 138–147 (1991). https://doi.org/10.1007/BF02528099

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